SA is an approved, easy technique and dependable and appears to be a possible replacement for GA in pediatric patients. However, it still remains relatively misspent if compared to GA in children in most institutions. Pediatric spinal anesthesia has manifested as a cautious substitute to conventionally administered general anesthesia as it avoids the polypharmacy associated with GA and also it prevents the incidence of postoperative respiratory complications.

SA is universally accepted in the clinical practice of anesthesia. Despite it producing excellent operating conditions with uniformly distributed analgesia and good neuromuscular blockade, its effect is short lived which is more in children than adults because of its efficient pharmacokinetics. Either potent systemic opioid analgesics are needed to extend the analgesia or intrathecal adjuvants are added to local anesthetics to prolong the analgesia. Systemic opioids are usually associated with a high incidence of respiratory depression, nausea, vomiting, itching, and urinary retention, so intrathecal adjuvants are preferred, devoid of such aftermath (Giaufre 2000; Kokki 1992).

Nickel et al. (2005) applied EMLA cream to the lumbar puncture area and IV cannulation site an hour prior to arrival in the operation room (not licensed for preterm < 37 weeks) and explained that good dermal analgesia might avoid the need for sedation in some children. In younger infants, ignorance acts as a prevention against panic, but older children require some premedication for easy parental separation, IV cannulation, and spinal puncture. Harnik et al. (1986) used midazolam, atropine, and ketamine alone or in combination by various routes (oral/rectal/IM) to provide sedation and anxiolysis. In our study, we applied EMLA cream at the site of IV cannulation and lumbar puncture an hour before the patient was taken to the operation theater irrespective of age.

Lopez et al. (2012) explained that during surgery under spinal anesthesia, it is important to soothe pediatric patients to prevent them from moving their bodies or bawling. Performing a spinal puncture in a struggling and agitated child might injure delicate neurovascular structures. SA by itself has sedative effects, probably due to a decrease in afferent input to the reticular activating system. Most children required additional sedation with ketamine, midazolam, thiopentone, propofol, halothane, sevoflurane, or nitrous oxide (Kokki et al. 2000a; Singh et al. 2010a; Ecoffey et al. 2010), while many infants were soothed with flavored pacifiers or sucrose-dipped dummy dip (Kokki 2012), before giving spinal blocks.

In our study, procedural sedation was given with ketamine 0.5 mg/kg BW IV with O2 and sevoflurane for 3 min, whereas Singh et al. (2010a) used ketamine in a dose of 0.4 mg/kg BW with ketamine infusion vs. propofol induction and infusion. To counter the gestures and activities during surgery and anesthesia procedure, they used propofol 2 mg/kg BW as induction and an additional 1 mg/kg bolus; Brown et al. (2012) continued propofol in the dose of 25–50 μg/kg/min in contrast to 20–50 μg/kg/min by Puncuh et. al. (2004) in pediatric patients.

Gerber et al. (2000) studied spinal and caudal anesthesia in ex-premature babies. Harnik E. V. et al. (1986) studied spinal anesthesia in premature infants recovering from respiratory distress syndrome. Abajian et al. (1984) studied spinal anesthesia for surgery in high-risk infants, whereas Ze’evshenkman et al. (2002) studied 62 premature and former premature or young infants. In our study, we included the children in the ASA I and II physical status and were of 3–13 years, which was in correlation with Parag et al. (2019) who studied children aged 3–8 years, and Blaise et al. (Rice and Britton 1989) studied in 7 months–13 years, H. Kokki et al. (2007) in 10–15 years, and Jambure (2013) studied in 3–12 years, which was similar to our study.

Alan Rochette et al. (2004) studied spinal anesthesia with different doses of clonidine and concluded that 1 μg/kg of clonidine increased the duration of blocks twofold when compared with plain isobaric bupivacaine. This dose of clonidine was not associated with hemodynamic or respiratory alterations, whereas 2 μg/kg was associated with more side effects with the same duration of blockade. Bang et al. (Bang-vojdanovski 1996), Lindo et al. (Rice and Britton 1989), and E. Giaufre (2000) used clonidine in a dose of 1 μg/kg without any hemodynamic instability or high spinal. We had similar observations in our study. The reason could be that the large volume/kg BW of cerebrospinal fluid in children allows a greater volume of distribution in the intrathecal space. Hypotension is also prevented by the immaturity of the sympathetic nervous system in children.

In our study, we preloaded the patient with Ringer lactate at 10 ml/kg, and none of the patients had hypotension which is comparable with the studies of Blaise et al. (1986) and Kokki and Hendolin (2000) (Brown 2012) where they preloaded with crystalloid 5–10 ml/kg. On the contrary, N. Jambure (2013) and Junkin et al. (2011) did no preloading in their studies with no reported hypotension.

The addition of clonidine to bupivacaine as an adjuvant resulted in the early onset of sensory block 3.16 ± 1.4162 min compared to bupivacaine alone, 4.8 ± 1.54 in the study by Jambure (2013) and similar in (Kaabachi et al. 2007). All these block characteristics were statistically significant on the comparison (p < 0.0000001) which co-related with our study where there was earlier onset of sensory block in group BC (3.04 ± 1.5) when compared to group B (5.01 ± 0.30) with a p-value of 0.0001. Similarly, the onset of motor block was also earlier in group BC 3.81 ± 0.38 min when compared with group B 6.47 ± 4.66 min with a p-value of 0.0028.

Kokki and Hendolin (2000) achieved an average segmental level of blockade of T4 with a lower dose and T5–6 with a higher dose. They used transcutaneous electrical stimulation to check the level of the spinal blockade. In contrast, none of the patients in our study, belonging to either group, demonstrated a level higher than T5. Children in group B demonstrated consistently higher levels of sensory blockade; 14 (46.66%) patients achieved T6 in group B, whereas 14 (46.66%) patients achieved T8 in group BC. The testing was done by the pinprick method.

Duration of analgesia was considered as the interval from the time of intrathecal injection to the time when analgesia was demanded postoperatively. The requirement for rescue analgesia is reduced by deep analgesia provided by intrathecal clonidine, which also extends the period until the sensory block’s regression and the recuperation of the motor block (Filos et al. 1994). The duration of the block was 181 ± 59 min in the plain isobaric bupivacaine group as compared to 252 ± 79 min in the clonidine group in the study done by Kaabachi et al. (2007). Kumar Parag et al. (2019) (Kokki and Hendolin 2000) also reported profound analgesia with prolonged time to regression of the sensory block and recovery of motor block, with decreasing need of rescue analgesia as compared to intrathecal fentanyl which co-related with our study where group BC provided the smooth and prolonged analgesia of 391.33 ± 33 min as compared to group B where analgesia lasted for only 194.5 ± 28 min which was statistically significant with p = 0.0001.

In our study, statistically significant differences in VAS were found from 30 min onwards until the rescue analgesia was given. They were very low in group BC as compared to group B which is co-related with the studies done by N. Jambure (2013).

The results of the study done by Rochette et al. (2004), Batra et al. (2010b), and Cao et al. (2011) clearly marked the effectiveness of intrathecal clonidine as a subtle sedative. The patients showed a response on gentle excitation. Statistically, we see clonidine sedation scores were highly convincing. In all patients, SpO2 was maintained at more than 90%. Mean sedation scores were also higher in group B than in group A (Cao et al. 2011; Singh et al. 2010b; De Sarro et al. 1987) and significant statistically i.e., ≤ 0.0000001. Ramsay sedation scores in our study were significant from 5 min to 3 h after the subarachnoid block. It showed group BC patients were more sedated than group B, but none of the patients in either group required supplemental oxygen, and SpO2 was above 97% at all times.

Due to the sympathetic fiber block, cardiovascular changes, reduction in heart rate, and fall in blood pressure are common corporal reactions during spinal anesthesia. As cardiovascular stability in children is good (Dohi and Naito 1979), spinal anesthesia is well tolerated by infants with few general autonomic alterations. (Bang-vojdanovski 1996) Being a centrally acting drug, clonidine easily crosses the blood-brain barrier and stimulates the central alpha-2 receptors. This decreases norepinephrine release and reduces sympathetic outflow to the heart and vascular system, which causes bradycardia hypotension and reduces peripheral vascular resistance.

None of the patients had significant bradycardia as reported by H. Kokki (2007), G. A. Blaise (1986), and Junken et al. (1933) where the mean heart rate was less in group 1 as compared to group 2, reached statistical significance after 10–40 min of skin incision, which was quite similar to our study and which also showed no significant difference among the two groups.

Mean arterial pressure in our study showed no significant difference among the two groups, except at the 5-min time mark where the p-value is 0.001. This suggests that there was no statistically or clinically significant change in the mean arterial pressure. It correlated with the studies of Hannu Kokki (2007), N. Jambure (2013), Blaise et al. (1986), Junken et al. (1933), and Kumar et al (2019).

Kumar et al. (2019) reported bradycardia (heart rate dropped to 60) in 3 children in group 1 and none of the children in group 2, which was treated with atropine. N. Jamubure (2013) reported bradycardia in 2 patients in clonidine group 1 patient in bupivacaine alone which responded to intravenous atropine 0.02 mg/kg. In our study, only one patient (33.33%) in the BC group had bradycardia which was treated with intravenous atropine.

Kumar et al. (2019) found that when a propofol bolus was given in reaction to an intraoperative movement, there was the majority of desaturation incidences seen in group 2. Nevertheless, at no point was the SpO2 of any patient recorded lower than 90% and so were the complications such as apnea and respiratory obstruction which occurred post-propofol bolus administration, resulting in deep sedation. This underscores the significance of intraoperative respiratory monitoring and the provision of additional oxygen to every patient undergoing regional anaesthesia with sedation. None of the patients in our group had desaturation, and all the patients in either group maintained O2 saturation equal to or more than 97%.

Kaabachi et al. (2007) reported hypotension was more frequent, 29% in the clonidine group and 17% in the control group, while hypotension incidence was 1–10% in adolescents with spinal anesthesia as reported by others (Kokki and Tuovinen 1998; Puncuh et al. 2004; Bang-vojdanovski 1996; Kokki and Hendolin 2000). None of the patients in our group had hypotension which could be well related to preloading with ringer lactate 10 ml/kg.

PDPH was thought to be rare in children < 10 years of age, because of low CSF pressure, highly elastic dura, and non-ambulation. Lately, it was reported in children as young as 2 years, suggesting that its occurrence is independent of age (Nickel et al. 2005) Overall incidence of 4–5% (as in adults) has been reported in 2–15 years age group (Kokki et al. 1998; Kokki et al. 2000b) Symptoms were mild. Studies reported a similar incidence of PDPH with pencil point and cutting needles (Hennaway et al. 2009) and a lesser incidence with pencil point (0.4% vs. 5%) (Junkin 1933). None of the patients in our study reported PDPH.